<<Disclaimer: Verify this information before applying it to your situation.>>
Below I share 4 ways that oxalate levels in the body might
be raised (1. a genetic predisposition, 2. low levels of
oxalate-degrading bacteria, 3. a vitamin B6 deficit, or 4.
a bowel dysfunction).
1. The only well-documented way that oxalate levels have
been shown to become dangerously high is through a genetic
predisposition:
Genetic hyperoxaluria – disease characterized by
progressive kidney failure due to renal deposition of
calcium oxalate. The disease is caused by a deficiency of
alanine:glyoxylate aminotransferase (AGT) which catalyzes
the conversion of glyoxylate to glycine. When AGT is
absent, glyoxylate is converted to oxalate which forms
insoluble calcium salts that accumulate in the kidney and
other organs.
Reference: Any medical dictionary. Recent review published
in Mol Genet Metab. 2004 Sep-Oct;83(1-2):38-46.
2. Some bacteria “eat” (degrade) oxalates, so when an
antibiotic is administered, the person’s oxalate levels
may spike. That's why some patients have flare-ups after
they take an antibiotic.
Oxalate degradation by the anaerobic bacterium Oxalobacter
formigenes is important for human health, helping to
prevent hyperoxaluria and disorders such as the
development of kidney stones. Oxalobacter formigenes and
Its Potential Role in Human Health
Sylvia H. Duncan et al. Applied and Environmental
Microbiology, August 2002, p. 3841-3847, Vol. 68, No. 8.
On the up-side, lactobacillus has been shows to degrade
oxalates in dogs and cats, reference: J.S. Weese et al. /
Veterinary Microbiology 101 (2004) 161–166.
3. Excess oxalate levels have also been shown to be a
result of vitamin deficiency (in particular vitamin B6):
Vitamin B6 reference: SAORI NISHIJIMA, KIMIO SUGAYA,
MAKOTO MOROZUMI, TADASHI HATANO and YOSHIHIDE OGAWA,
Hepatic Alanine-glyoxylate Aminotransferase Activity and
Oxalate Metabolism in Vitamin B6 Deficient Rats, The
Journal of Urology, Volume 169, Issue 2, February 2003,
Pages 683-686
4. According to the recent listserv post referencing Susan
Owens’ autism work, there is a known link between excess
oxalates and bowel dysfunction. I don’t doubt this claim,
makes sense to me, but there is in fact very little
scientific research to substantiate it.
“Irritable bowel disease (IBD) can increase the risk of
forming calcium oxalate kidney stones. This observation
can be explained by the fact that when the gut is
inflamed, when there is poor fat digestion (steatorrhea),
when there is a leaky gut, or when there is prolonged
diarrhea or constipation, excess oxalate from foods can be
absorbed by the GI tract.” – Susan Owens, MAIS, RA, Autism
Oxalate Project
References: An interesting paper with few references to
oxalate research written by Mrs. Susan Owens on leaky gut
and the low-oxalate diet is available online:
http://www.usautism.org/USAAA_Newsletter/mechanisms_behind_the_leaky_gut.pdf
Other than Susan’s work, there is little mention in the
peer-reviewed literature specifically linking high oxalate
levels to bowel dysfunction except for a few papers on
short bowel syndrome (SBS) which most commonly results
after bowel resections for Crohn’s disease, the first of
which was published in 1992:
Nightingale JMD, Lennard-Jones JE, Gertner DJ, et al.
Colonic preservation reduces the need for parenteral
therapy, increases the incidence of renal stones but does
not change the high prevalence of gallstones in patients
with a short bowel. Gut 1992;33:1493-1497
In 1980 it was shown that the colon is the presumed site
of enhanced oxalate absorption in patients with
steatorrhea (a common symptom of celiac disease): Oxalate
uptake by everted sacs of rat colon. Biochim Biophys Acta.
1980 Mar 13;596(3):404-13.
Visit the Celiac Web Page at Http://www.enabling.org/ia/celiac/index.html
Archives are at: Http://Listserv.icors.org/SCRIPTS/WA-ICORS.EXE?LIST=CELIAC
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